As the primary U.S. funding source of Alzheimer's
research, the government's National Institute on
Aging strives to guard against the possibility that
scientific orthodoxy could limit the search for
treatments and prevention of Alzheimer's disease.
NIA scientists and grantees, including some of the
scientists quoted in Ms. Begley's columns, are deeply
involved in discussions on alternative theories
to the amyloid hypothesis.
The NIA supports major projects on the proteins
tau and apolipoprotein E,
antioxidants and inflammation. Further, important
initiatives in imaging
and in genetics look considerably beyond amyloid's
Alzheimer's disease.While it is true the role of
amyloid and related brain plaques is a
significant focus of study, investigators in Alzheimer's
today actively pursue many other exciting fronts
All of us at the NIH have a mission
to reduce disease and disability. In
the case of Alzheimer's, until cause and cure are
established, we are open
to rigorous testing of all credible theories as
to why and how this disease
develops. Everyone holds convictions, some might
say biases, but the NIH is
committed to ensuring bias does not stand in the
way of progress against
the devastation of Alzheimer's disease.
Richard J. Hodes, M.D.
Director, National Institute on Aging
National Institutes of Health
U.S. Department of Health and Human Services
I very much appreciated Sharon Begley's articles
on Alzheimer's disease research and the funding
bias in favor of amyloid research to the exclusion
of alternative theories ("Is Alzheimer's Field
Blocking Research Into Other Causes?", April
9, and "Scientists World-Wide Battle a Narrow
View of Alzheimer's Cause," April 16).
These articles honestly expose how
scientists, even those dedicated to intellectual
honesty in scientific investigation, can become
so committed to one set of ideas that their eyes
are clouded.As I have studied Alzheimer's disease,
initially as an outsider from the field of cardiovascular
disease, I have come to realize the condition would
be better termed Alzheimer's diseases.
Such complex illnesses as Alzheimer's
are often the product of multiple agents interacting
through various pathways to cause pathology. Undoubtedly
amyloid does indeed play a key role in the pathogenesis
of some forms of Alzheimer's, but in other
cases different agents may be the key mediators
of the process. Clearly,
the strongest genetic contributor of this and other
is the occurrence of the apolipoprotein E4 allele.
It may or may not have
its impact on neurobiology through amyloid, and
it is certainly not the
only cause of this disease. However, this protein
and others deserve to be
studied without bias.
Ms. Begley's articles underscore
the important concept that, of all human
endeavors, science above all must be free to explore
ideas and open up new
areas of inquiry. There is no place for narrow-mindedness
one's own turf if we are to solve complex diseases
and advance prevention
and treatment of disorders plaguing humankind.
Robert W. Mahley, M.D., Ph.D.
J. David Gladstone Institutes
Professor, Pathology & Medicine
University of California